Detecting and responding to environmental perturbations are important for all living organisms. Our long-term goal is to understand the mechanisms multicellular eukaryotes use for sensing and cellular signaling of adverse environments. Our work has focused on the Salt Overly Sensitive (SOS) pathway for Na+ and K+ homeostasis in the model multicellular organism Arabidopsis thaliana. In the SOS pathway, a myristoylated calcium-binding protein, SOS3, senses cytosolic calcium changes elicited by exposure to high Na+. SOS3 with bound calcium physically interacts with and activates the protein kinase SOS2. The SOS3-SOS2 kinase complex phosphorylates and activates the transport activity of the plasma membrane Na+/H+ exchanger SOS1. The coordinated regulation of SOS1 and other ion transporters restores ion homeostasis under high salt conditions. Besides functioning as a transporter, SOS1 also plays a regulatory role in oxidative stress management. High salt conditions trigger the re-localization of Radical- induced Cell Death 1 (RCD1), a transcriptional regulator of oxidative stress response, from the nucleus to the cytoplasm to interact with the C-terminal cytosolic tail of SOS1. We also identified two putative upstream protein kinases that are likely involved in SOS2 activation and discovered several small non-coding RNAs that are regulated by salt and oxidative stress and function in salt response pathways. The current proposal addresses the following specific aims: 1) Continued investigation of the regulatory function of SOS1. A variety of biochemical, cell biological, molecular and genetics approaches will be used to determine the role of SOS1 in sensing Na+ and generating a micro-domain Ca2+ signal for the SOS pathway. We will also analyze the role of SOS1 in oxidative stress management and elucidate the mechanism of subcellular redistribution of RCD1 in response to salt and oxidative stresses. 2) Investigation of the role of putative upstream kinases in SOS2 activation. 3) Functional analysis of small non-coding RNAs in regulating the expression of SOS1 and other salt-tolerance determinants and their role in epigenetic regulation of responses to the environment.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM059138-13
Application #
7821432
Study Section
Special Emphasis Panel (ZRG1-CSRS-N (01))
Program Officer
Maas, Stefan
Project Start
1999-05-01
Project End
2010-12-31
Budget Start
2010-05-01
Budget End
2010-12-31
Support Year
13
Fiscal Year
2010
Total Cost
$41,310
Indirect Cost
Name
University of California Riverside
Department
Genetics
Type
Schools of Earth Sciences/Natur
DUNS #
627797426
City
Riverside
State
CA
Country
United States
Zip Code
92521
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